Cleft palate is one of the most prevalent congenital malformations seen in man. Corticosteroid-induced cleft palate has been the object of extensive research; however, the mechanism by which this birth defect is generated has not been firmly established. The objectives of the proposed research deal with the possible mechanism by which cortisone delays the movement of the palatine shelves, resulting in a decreased possibility for fusion and a cleft of the secondary palate. Because of the ease of detecting it and also because of its present or absent nature, this defect lends itself to many aspects of experimental teratogenesis. Palatal shelves at various stages of embryogenesis will be isolated from normal mothers and from mothers treated with cortisone on the eleventh to fourteenth days of pregnancy. Both normal and cortisone-treated mothers will receive radioactive glucosamine 24 hrs prior to sacrifice. The content of palatal glycosaminoglycans will be determined in both normal and abnormal palatal shelves at several stages of palatogenesis. The level of certain enzymes involved in the synthesis of the palatal glycosaminoglycans will also be determined at similar stages of palatogenesis. The effect of hyaluronic acid on palatal cells in culture will be studied, in order to determine whether this glycosaminoglycan plays a role in mesenchymal cell migration and shelf fusion by virtue of a stimulation of the cells biosynthetic capacities.